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Deletion of 17p and Amplification of the int-2 Gene in Esophageal Carcinomas¹

Radiation Biology Center (T. W., K. I., M. Ik.) and First Department of Surgery, Faculty of Medicine (T. W., M. Im., Y. S., T. T.), Kyoto University, Yoshida-Konoecho, Sakyo-ku, Kyoto 606, Japan

We have analyzed allelic deletion at 23 loci on 18 different chromosomes in 35 esophageal squamous cell carcinoma tissues by using restriction fragment length polymorphism markers. Loss of heterozygosity was detected on chromosomes 2, 3, 6, 7, 11–14, 16–18, 21, and 22, while no loss was detected on chromosomes 1, 4, and 8–10. Only the loss of chromosome 17p was detected with high frequency (45%), and losses on other chromosomes had frequencies of <22%. These losses with low frequencies might be random losses caused by chromosomal rearrangement during the course of tumor development and progression. On the contrary, the loss of 17p might play an important role in the development of esophageal squamous cell carcinoma, such as inactivation of a tumor suppressor gene. Amplification of the int-2 gene was observed in 39% of the tumors. However, no significant relationship between int-2 amplification and the deletion of any chromosome was detected.

¹ This study was supported in part by a grant from the Ministry of Education, Science and Culture, Japan.

² To whom requests for reprints should be addressed.

Received 10/ 4/90. Accepted 2/ 1/91.

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